ArticleInfection and immunity2011
Molecular basis of immunity to rickettsial infection conferred through outer membrane protein B.
Article in Infection and immunity, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
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Who cites it
43 citing papers in PubMed, 67 citations in OpenAlex.
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- Transposon mutagenesis of Rickettsia felis sca1 confers a distinct phenotype during flea infection.PLoS pathogens · 2022Article
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- Spotted Fever GroupMicrobiology spectrum · 2021Article
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- Contribution of classical complement activation and IgM to the control of Rickettsia infection.Molecular microbiology · 2021Article
- Rickettsia conorii survival in THP-1 macrophages involves host lipid droplet alterations and active rickettsial protein production.Cellular microbiology · 2021Article
- Host EPAC1 Modulates Rickettsial Adhesion to Vascular Endothelial Cells via Regulation of ANXA2 Y23 Phosphorylation.Pathogens (Basel, Switzerland) · 2021Article
- Mediterranean Spotted Fever: Current Knowledge and Recent Advances.Tropical medicine and infectious disease · 2021Review
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- Significant Growth byPathogens (Basel, Switzerland) · 2021Article
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- The neglected challenge: Vaccination against rickettsiae.PLoS neglected tropical diseases · 2020Review
- Comparative Analysis of Infection byPathogens (Basel, Switzerland) · 2020Article
- A new role for host annexin A2 in establishing bacterial adhesion to vascular endothelial cells: lines of evidence from atomic force microscopy and an in vivo study.Laboratory investigation; a journal of technical methods and pathology · 2019Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Pathogenic rickettsiae are the causative agents of Rocky Mountain spotted fever, typhus, and other human diseases with high mortality and an important impact on society. Although survivors of rickettsial infections are considered immune to disease, the molecular basis of this immunity or the identification of protective antigens that enable vaccine development was hitherto not known. By exploring the molecular pathogenesis of Rickettsia conorii, the agent of Mediterranean spotted fever, we report here that the autotransporter protein, rickettsial outer membrane protein B (rOmpB), constitutes a protective antigen for this group of pathogens. A recombinant, purified rOmpB passenger domain fragment comprised of amino acids 36 to 1334 is sufficient to elicit humoral immune responses that protect animals against lethal disease. Protective immunity requires folded antigen and production of antibodies that recognize conformational epitopes on the rickettsial surface. Monoclonal antibodies (MAbs) 5C7.27 and 5C7.31, which specifically recognize a conformation present in the folded, intact rOmpB passenger domain, are sufficient to confer immunity in vivo. Analyses in vitro indicate this protection involves a mechanism of complement-mediated killing in mammalian blood, a means of rickettsial clearance that has not been previously described. Considering the evolutionary conservation of rOmpB and its crucial contribution to bacterial invasion of host cells, we propose that rOmpB antibody-mediated killing confers immunity to rickettsial infection.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.